Angiopoietin-2: A Key to Understanding Sepsis and Its Pulmonary Sequelae?Ji Young Lee1,2,3* and Edmund J. Miller1,2,4
- *Corresponding Author:
- Ji Young Lee, MD
Department of Pulmonary Critical Care Medicine
University of South Alabama, USA
E-mail: [email protected]
Received date: December 27, 2013; Accepted date: February 06, 2014; Published date: February 10, 2014
Citation: Lee JY, Miller EJ (2014) Angiopoietin-2: A Key to Understanding Sepsis and Its Pulmonary Sequelae? J Pulm Respir Med 4:172. doi:10.4172/2161-105X.1000172
Copyright: © 2014 Lee JY, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Sepsis remains a major cause of morbidity and mortality especially in the older individual. In the US alone, sepsis occurs in approximately 750,000 individuals per year and ranks as the tenth leading cause of death. A major complication of sepsis is organ failure, with the lung being one of the first organs to fail. Moreover, sepsis is the most common risk factor for Acute Lung Injury (ALI) and approximately 50% of individuals with sepsis subsequently develop ALI. Despite its importance, the pathophysiology of sepsis remains unclear. Angiopoietin-2 (Ang-2) is a component of pathways involved in endothelial survival and maintenance of a quiescent state of the vascular system. The functional significance of Ang-2 remains to be fully elucidated, but the evidence thus far suggests that it may be key to a better understanding of the vascular dysfunction and associated organ failure that are so devastating in sepsis. However, the assessment of the cellular release of Ang-2 is not without difficulty. In this brief review, we discuss the relevance of Ang-2 to the endothelial dysfunction associated with the severe inflammatory response in sepsis, and why Ang-2 may not be just a biomarker, but may play a critical role in the pathology. In addition, we discuss some of the reasons why particular sepsis models may present confusing data with respect to Ang-2 involvement.